Myocardial Infarction - Weber State University Myocardial Infarction •A myocardial infarction refers

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  • Myocardial Infarction

    Symbree Minniear

  • Myocardial Infarction

    • A myocardial infarction refers to the death of myocardial muscle cells that occurs when a substantial decrease or complete disruption of blood flow through a coronary artery deprives the downstream tissue of oxygen for an extended period.

    • In an MI, an area of the myocardium is permanently destroyed and cannot be .

  • Epidemiology

    • Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one.

    • Coronary heart disease caused 1 of every 6 deaths in the United States in 2008.

    • About every 34 seconds, someone in the United States has a myocardial infarction.

  • Symptoms

    • Pain is the most common symptom in patients’ experience a MI.

    • Pain can be experienced in your arms, shoulder, neck, teeth, jaw, abdomen, or back.

    • It may feel like a tight band around the chest, bad indigestion, like something is sitting on your chest, or squeezing.

    • Undue fatigue

    • Palpitations

    • Dyspnea

    • Anxiety

    • Cough

    • Fainting

    • Light-headedness, dizziness

    • Nausea or vomiting

    • Profuse sweating

    • Confusion

  • Laboratory Diagnosis

    • Blood analysis can be performed to determine whether tissue damage has occurred to the myocardium.

    ▫ Polymorphonuclear leukocytes and erythrocyte sedimentation rates are both indicative of myocardial damage.

    • Myocardial injury can also be recognized by the appearance of various cardiac biomarkers that are released when the myocardial walls lose their integrity.

    ▫ Biochemical markers such as troponin (I and T), creatinine kinase (CK) and its isoenzyme CK-MD, and lactate dehydrogenase (LDH).

  • Tests and Evaluation

    • Electrocardiography (ECG): ▫ Patients presenting with an acute transmural MI have

    ECG changes that include hyperpolarization of the T waves and ST-segment elevation.

    ▫ Patients experiencing a subendocardial MI typically demonstrate ST-segment depression.

    • Echocardiography: ▫ Provides information regarding wall motion and blood

    perfusion. ▫ Two-dimensional echocardiography is used to visualize

    the left ventricular walls and assess the amount of movement.

  • Tests and Evaluation

    • Multiple-gated analysis (MUGA):

    ▫ Uses technetium-99m stannous pyrophosphate, which tags to red blood cells.

    ▫ By imaging tagged red blood cells wall motion and ejection fraction can be assessed.

    • Computed tomography (CT) and magnetic resonance imaging (MRI):

    ▫ May also be used to assess ventricular wall motion.

    • Radionuclide imaging:

    ▫ Are used to assess either blood flow defects or wall motion abnormalities.

  • Complications

    • Arrhythmias can occur if the myocardium is damaged due to an MI.

    • Depending on the amount of damaged tissue the heart may not be able to adequately pump blood to the body, which may lead to heart failure.

    • Areas of heart muscle weakened by a heart attack can rupture, leaving a hole in part of the heart.

    • Heart valves damaged during a heart attack may develop severe, life-threatening leakage problems.

  • Treatment

    Acute Treatment Chronic Treatment

    • Sublingual nitroglycerin and morphine

    • Percutaneous coronary intervention (PTCA)

    • Coronary artery bypass graft surgery (CABG)

    • Revascularization

    • Thrombolytic therapy

    • Angioplasty

    • Bed rest

    • Regular physical activity • β-blockers • Angiotensin-converting

    enzyme inhibitors (ACE) • Aspirin • Anticoagulation therapy • Lipid management • Calcium channel blockers • Antiplatelet therapy • Antiarrhythmic therapy

  • Effects of MI on Ability to Exercise

    • Reduced level of cardiorespiratory fitness approximately 50-70% of age and gender predicted.

    • Reduced oxygen transport capacity due to diminished cardiac output.

    • Decrease in ejection fraction and stroke volume.

    • Increased heart rate due to a decrease in stroke volume.

    • Exercise-induced ventricular arrhythmias.

  • Effects of Medications on Exercise

    • β-blockers: ▫ Decrease submaximal and maximal heart rate and

    sometimes exercise capacity. ▫ Prevent or delay signs or symptoms of myocardial

    ischemia and increase exercise tolerance in clients with exertional angina.

    • Vasodilators, ACE inhibitors, and angiotensin recep0tor blockers: ▫ May be subject to hypotensive episodes during the

    postexercise period unless an adequate cool down period is allowed.

  • Effects of Medication on Exercise

    • Calcium channel blockers: ▫ May decrease the heart rate response at rest and

    during exercise and prevent or delay manifestations of myocardial ischemia.

    • Central nervous system—active drugs: ▫ Can have attenuating effects on heart rate and

    blood pressure during exercise.

    • Alpha receptor blockers: ▫ Significantly lower systolic and diastolic blood


  • Effects of Medications on Exercise

    • Antiarrhythmic agents: ▫ Can cause false negative or false positive test results.

    • Digitalis: ▫ ST-segment depression can be induced or

    accentuated during exercise in persons with or without heart disease.

  • Effects of Exercise Training

    • Increased maximal oxygen consumption (VO2max).

    • Improvement in the ventilatory response to exercise.

    • Improvement in the anaerobic threshold.

    • Relief of angina symptoms secondary to reductions in heart rate or blood pressure.

    • Modest decreases in body weight, fat stores, blood pressure, total blood cholesterol serum triglycerides, and LDL- cholesterol.

    • Increases in the “antiatherogenic” high- density lipoprotein (HDL) cholesterol subfraction.

  • Effects of Exercise Training

    • Improved psychosocial well-being and self- efficacy.

    • Protection against the triggering of MI by vigorous physical exertion.

    • Decreased coronary inflammatory markers.

    • Increased numbers of endothelial progenitor cells and circulating angiogenic cells

    • Decreased blood platelet adhesiveness, fibrinogen, and blood viscosity and increased fibrinolysis.

    • Increased vagal tone and decreased adrenergic activity.

    • Increased heart rate variability.

  • Exercise Testing

    • Graded exercise testing are used in post-MI patient to evaluate prognosis and functional status.

    • Exercise protocol can be submaximal or symptom limited.

    • Treadmills or cycle ergometers are the most common modes of testing.

    • The protocol is low level, with work rate increments of 1 to 2 METs every 2 to 3 min.

    • Blood pressure, ECG and symptom monitoring should be performed throughout the exercise test.

  • Exercise Testing

    Submaximal Testing Symptom Limited Testing

    • Common criteria for test termination include:

    ▫ A peak heart rate between 120 and 130 bpm

    ▫ Achieving 70% of predicted maximal heart rate.

    ▫ A peak work rate of 5 METs

    • These tests are designed to continue until the patient demonstrates signs or symptoms such as:

    ▫ Angina

    ▫ ST-segment depression

    ▫ Hypotension

    ▫ Ventricular arrhythmias

    ▫ Fatigue

  • Exercise Prescription Modes Goals Intensity/Frequency/

    Duration Time

    to goal

    Aerobic Large muscle activity

    •Increase aerobic capacity •Decrease BP & HR response to submaximal exercise •Decrease submaximal myocardial VO2 demand •Decrease CAD risk factors •Increase ADLs

    •RPE 11-16/20 •40-80% VO2mx or HR reserve •≥3 days/week •20-60 min/session •5-10 min of warm-up and cool- down activities

    4-6 months

    Strength Circuit Training

    •Increase ability to perform leisure and occupational activities and ADLs •Increase muscle strength and endurance

    •30-40% 1RM (upper body), 50- 60% (lower body) •2-3 days/week •2-4 sets of 12-15 reps •8-10 different exercises •Arbitrary weight increase

    4-6 months

    Flexibility Upper & Lower body ROM

    Decrease risk of injury •Static stretches: hold for 10-30 s •2-3 days/week

    4-6 months

  • Conclusion

    • Regular exercise has been shown to mediate the atherosclerotic process and therefore to protect against both initial and subsequent MIs, as well as mortality from all causes.

    • Therefore, habitual exercise training is an accepted and important part of the rehabilitative process for patients who have had an MI.

  • References

    • ACSM. 2010. ACSM’s guidelines for exercise testing and prescri